Interaction between nitric oxide and prostaglandin synthesis in the acute phase of allergic conjunctivitis

F. Meijer , C. Tak , N.J. van Haeringen , A. Kijlstra
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引用次数: 19

Abstract

Both nitric oxide and prostaglandins induce vasodilatation which is an important feature of local inflammation. The purpose of the study described here was to investigate a possible interaction between these two types of mediators in an experimental model of allergic conjunctivitis. A conjunctival allergic reaction was induced with antigen in sensitized guinea pigs. Conjunctival vascular permeability changes were evaluated with the prophylactic use of an inhibitor of nitric oxide synthase (L-NAME) and a cycloxygenase inhibitor (indomethacin). To study a possible interaction between nitric oxide and prostaglandin synthesis in the acute phase of allergic conjunctivitis, the levels of nitrite and PGE2 were determined in lavage fluid. The prophylactic use of L-NAME on the formation of conjunctival edema in response to topical PGD2 administration was studied by measurement of albumin levels in lavage fluid. Both nitric oxide and PGE2 are synthesized in response to antigen provocation and after histamine administration. Nitric oxide and PGE2 are produced simultaneously in the conjunctiva and they showed identical synthesis profiles in response to antigen provocation. Pretreatment with L-NAME inhibited the synthesis of PGE2 whereas exogenous administration of nitric oxide increased the level of PGE2 in lavage fluid. Prophylactic treatment with L-NAME significantly inhibited the PGD2 induced albumin extravasation. Nitric oxide seems to play an important role in the acute phase of allergic conjunctivitis it may stimulate PGE2 production and acts as a secondary mediator in PGD2 and histamine induced conjunctival edema.

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过敏性结膜炎急性期一氧化氮与前列腺素合成的相互作用
一氧化氮和前列腺素都能引起血管扩张,这是局部炎症的一个重要特征。本研究的目的是在过敏性结膜炎的实验模型中研究这两种介质之间可能的相互作用。用抗原诱导致敏豚鼠结膜过敏反应。通过预防性使用一氧化氮合酶抑制剂(L-NAME)和环氧合酶抑制剂(吲哚美辛)来评估结膜血管通透性的变化。为了研究过敏性结膜炎急性期一氧化氮与前列腺素合成之间可能的相互作用,我们测定了灌洗液中亚硝酸盐和PGE2的水平。通过测定灌洗液白蛋白水平,研究了L-NAME对PGD2局部给药后结膜水肿形成的预防作用。一氧化氮和PGE2都是在抗原激发和组胺给药后合成的。一氧化氮和PGE2在结膜中同时产生,它们在抗原激发下表现出相同的合成谱。L-NAME预处理可抑制PGE2的合成,而外源性一氧化氮可提高灌洗液中PGE2的水平。L-NAME预防性治疗可显著抑制PGD2诱导的白蛋白外渗。一氧化氮似乎在过敏性结膜炎的急性期发挥重要作用,它可能刺激PGE2的产生,并在PGD2和组胺诱导的结膜水肿中作为次级介质。
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